This CR3M monoclonal antibody reacts with human CCL3. CCL3, also known as MIP-1 alpha (Macrophage Inflammatory Protein 1 alpha), is a member of the CC- subfamily of chemokines and is most closely related to CCL4, or MIP-1 beta. These proteins play critical roles in the recruitment of leukocytes to the site of inflammation. While both CCL3 and CCL4 will attract monocytes, macrophages, and dendritic cells, CCL3 preferentially attracts CD8+ T cells, while CD4+ T cells are more responsive to CCL4. In addition to its chemotactic functions, CCL3 induces inflammatory cytokine secretion, mast cell degranulation, and NK cell activation. It has also been reported to inhibit hematopoetic stem cell proliferation and may be responsible for the maintenance of these cells in a quiescent state.

CCL3 signaling is mediated by the G protein-coupled receptors CCR1, CCR4, and CCR5, which are shared with CCL4 and CCL5 (RANTES). CCR5 is the primary co-receptor for HIV entry, which the virus binds through the gp120 envelope protein. All CCR5 ligands demonstrate potent inhibition of virus entry into the cell, both through steric hindrance of gp120-CCR5 interaction, and ligand-mediated receptor internalization.

This CR3M clone is specific to CCL3, with no detectable cross-reactivity to Human CCL4 (MIP-1 beta).